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musculoskeletal RDT > Systemic lupus erythematosus (SLE) > Flashcards

Systemic lupus erythematosus (SLE) Flashcards

1
Q

What type of disease is SLE?

A

It is a rare autoimmune disease

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2
Q

SLE is a part of a family of diseases- what are the other diseases in that family?

A
  • Rheumatoid arthritis
  • Sjogren’s syndrome
  • Dermatomyotis
  • Polymyositis
  • Systemic sclerosis
  • SLE
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3
Q

What is the gender ratio for SLE?

A

• Gender ratio M:F=1:9

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4
Q

At what age to SLE’s present?

A

15-40 years

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5
Q

Which ethnicities is SLE more prominent?

A

Afro-Carribean, Asian, Chinese

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6
Q

What is the prevalence of SLE?

A

4-280/100,000

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7
Q

What are the gene associations with SLE?

A

Genetic associations: with multiple genes implicated Fc receptors, IRF5, CTLA4, MHC class 2 HLA genes and complement deficiency- c1q and c3.

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8
Q

how does SLE present?

A

Malaise, fatigue, fever and weight loss. Accompanied by lymphadenopathy (abnormal size and shapes of lymph nodes).

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9
Q

What are the specific features of SLE?

A
  • Butterfly rash
  • Alopecia
  • Arthralgia- joint pain
  • Raynaud’s phenomenon
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10
Q

What are the additional pathological features of SLE?

A
  • Inflammation of the kidney, CNS, heart and lungs
  • Accelerated atherosclerosis
  • Vasculitis
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11
Q

What are some of the roles of B cells in the immune response

A
  • Antigen presentation
  • Antibody production
  • Activate antigen-presenting cell function
  • Regulate T cell activation anergy or differentiation
  • Produce cytokines
  • Regulate FDC differentiation
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12
Q

How is B cell function different in SLE?

A

In SLE genetic factors increase B cell reactivity so that it can directly result in autoantibody production and end-organ damage.
It can also increase the capacity of B cells to enhance the function of a variety of other cells.

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13
Q

What are the steps for the formation of autoantibodies

A

1) abnormal clearance of apoptotic cell material
2) dendritic cell uptake of autoantigens and activation of B cells
3) B cell Ig class switching and affinity mutation
4) IgG autoantibodies
5) Immune complexes
6) complement activation cytokine generation

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14
Q

What is the significance of the overactive B cells?

A

Overactive B cells are exposed to the autoantigens and the plasma cells begin to produce auto antibodies which form immune complexes. This deposits in tissues (mainly kidneys and skin) which then activates complement in the tissues.

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15
Q

How is SLE diagnosed?

A

1) Send serum to check for anti-nuclear antibodies (not diagnostic of SLE specifically)
2) Serum is then combined will cells and if ANA (antinuclear antibodies) are present, they will bind to the cell’s nuclear antigens. A fluorescently labelled antibody is added that binds to ANAs and you observe the pattern of attachment.

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16
Q

What are the 3 things you can test the serum with?

A

ANAs
Anti-dsDNA and Sm
Anti-Ro and /or La

17
Q

Name some other tests done to identify SLE?

A
  • Increased complement consumption- patients with active lupus will have more complement bound to immune complexes and so the blood complement will be low in active lupus
  • Anti-cardiolipin antibodies
  • Lupus anticoagulant
  • B1 glycoprotein
18
Q

What are the haematological tests done to diagnose SLE?

A
  • Lymphopenia, normochromic anaemia- SLE patients will present with autoimmune haemolytic anaemia- antibodies will bind to RBC surfaces and they are extravascularly removed in the spleen.
  • Leukopenia, AIHA, thrombocytopaenia
19
Q

What are the renal tests you can do to diagnose SLE?

A
  • Proteinuria, haematuria

* Active urinary sediment

20
Q

How do you assess the severity of SLE?

A

1) Identify pattern of organ involvement
2) Monitor function of affected organs-
• Renal- BP, U&E, urine sediment GFR
• Lungs/CVS- lung function tests, echocardiography
3) Identify the patterns of autoantibodies expressed
• Anti-dsDNA, anti-Sm- renal disease
• Anti-cardiolipin antibodies

21
Q

What are the clinical features of SLE

A
  • Wt loss, fatigue, malaise, hair loss
  • Alopecia
  • Rash
22
Q

What are the lab features of SLE?

A
  • ESR
  • Increased complement consumption
  • Increased anti-dsDNA
  • Other Abs e.g ANA and CRP poor indicators
23
Q

How are people with SLE split up into different categories?

A

People who have the disease are split into 3 groups:
1. MILD- joint pain some skin involvement- there is no sign of organ involvement
2. MODERATE- inflammation of other organs, pleurits, pericarditis, mild nephritis
3. SEVERE- severe inflammation in vital organs
• Severe nephritis
• CNS disease
• Pulmonary disease
• Cardiac involvement
• AIHA, thrombocytopaenia, TTP

24
Q

What is the treatment of mild SLE?

A

Paracetamol +/- NSAIDs and renal function is monitored
Hydroxychloroquine- for arthropathy, cutaneous manifestations, mild disease activity
Topical corticosteroids

25
Q

what is the treatment for moderate SLE (how do you know that the patient has moderate and not mild SLE)?

A

You know if they have moderate disease if there is failure of hydroxychloroquine/ NSAID and they start to get organ failure.
Moderate SLE indicates switch or topical  oral glucocorticoids:
• Initial high dose and titrate down
• High dose is needed to suppress disease activity but is also very toxic so can give the corticosteroids with steroid-sparing agents to lower the dose required.

26
Q

How is severe SLE treated?

A

Azathioprine- effective steroid-sparing agent comes with risk of neutropenia andbone marrow suppression so needs blood monitoring
Cyclophosphamide- severe organ involvement- affective in inducing remission. This leads to infertility.

27
Q

New treatments for severe SLE?

A

Mycophenolate mofetil- rate-limiting enzyme in purine synthesis. Lymphocytes are dependent upon de novo purine synthesis.
Rituximab- leads to depletion of B cells- effective in lupus nephritis

These drugs are as effective in inducing remission as cyclophosphamide. They are teratogenic drugs (cause congenital issues so don’t get pregnancy), but there is no effect on fertility.

28
Q

What is the survival like after treatment?

A

These treatments have 15-year survival:
• No nephritis 85%
• Nephritis= 60%

Prognosis is bad if black male with low socioeconomic status

29
Q

What are the 2 peaks of mortality?

A

There is an early peak in mortality in SLE and then a late peak:
• Early death- from renal failure, CNS disease, infection
• Late death- from MI or stroke

30
Q

What are the features you would see on a SLE blood film?

A
  • Shistocytes
  • Spherocytes
  • Teardrop cells
  • Few leukocytes and platelets
31
Q

What are the features from an SLE renal biopsy?

A
  • Hyper cellular there are more cells than normal.
  • Mesangial proliferation
  • Crescent development- inflammatory cells that have migrated into the glomerulus
  • Rapidly proliferation glomerulonephritis

musculoskeletal RDT (5 decks)

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